Loss of Sirt3 accelerates arterial thrombosis by increasing formation of neutrophil extracellular traps and plasma tissue factor activity

ConclusionsSirt3 loss-of-function enhances experimental thrombosisin vivo via an increase of neutrophil extracellular traps and elevation of TF suggesting thrombo-protective effects of endogenous Sirt3. Acute coronary thrombosis in STEMI patients is associated with lower expression levels ofSIRT3 andSOD2 in CD14+ leukocytes. Therefore, enhancingSIRT3 activity by pan-sirtuin activating NAD+-boosters may provide a novel therapeutic target to prevent or treat thrombotic arterial occlusion in myocardial infarction or stroke.
Source: Cardiovascular Research - Category: Cardiology Source Type: research